In puberty and adulthood

Increasing androgenic steroid secretion from the adrenals is defined as adrenarche and precedes puberty. Adrenarche is associated with increased growth of pubic and axillary hair independent of gonadal androgen secretion. Adrenal androgens include mainly dehydroepiandrostendione, its sulfate, and androstendione, but also other adrenal steroids have androgenic potential. Adrenocorticotropic hormone (ACTH) is a potent stimulator of adrenal androgen secretion; however, its potency relative to cortisol secretion is much less. Also, substances other than ACTH may modulate adrenal androgen secretion. These include estrogens, prolactin, growth hormone, gonadotropins and lipotropin. None of these appear to be the usual physiological modulator, although under some circumstances each may increase androgen production (Odell and Parker 1984). Adrenal androgen levels will continue to increase during adolescence until the third decade of life when a continuous and variable decrease will be prevalent.

Normal male puberty starts with the enlargement of testes and penis. Testicular volume increases from 1 to 2 cc prepubertally to 3 to 8 cc evenbefore pubic hairs start to appear and reaches 20-30 cc in adulthood. In addition to changes in secondary hair and genital changes, increasing testosterone concentrations produce other changes in most tissues of the body. The larynx increases in size and the voice deepens. Also bone mass and muscle strength increase, a growth spurt occurs, the erythrocyte cell mass increases, the skin thickens, and hair growth on the trunk is enhanced, as well as androgenic hair recession may occur. Sex steroids, and specifically testosterone may alter behaviour, and central nervous effects include stimulation of sexual libido and aggressiveness.

Testosterone in conjunction with FSH is an essential endocrine factor for sper-matogenesis in male mammals which acts directly on the germinal epithelium via the AR. During sex hormonal quiescence in prepuberty, germ cell proliferation is arrested until the juvenile phase. Testosterone alone can induce spermatogene-sis if administered during this period (Marshall etal. 1984). However, quantitative maintenance of the spermatogenic process cannot be achieved by testosterone alone, but needs the supportive action of FSH (Weinbauer and Nieschlag 1990, see also Chapter 5).

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